Evidence that thalidomide modifies the immune response of patients suffering from actinic prurigo

Background. Actinic prurigo (AP) is a photodermatosis with a restricted ethnic distribution, mainly affecting Mestizo women (mixed Indian and European). The lesions are polymorphic and include macules, papules, crusts, hyperpigmentation and lichenification. Thalidomide, an effective immunomodulatory drug, was first used successfully to treat AP in 1973. In this work we describe the effect that thalidomide had on TNF-α sera levels and on IL-4- and IFN gamma (IFNγ)-producing lymphocytes of actinic prurigo (AP) patients. Methods. Actinic prurigo patients were analyzed before and after thalidomide treatment. The percentage of IL-4+ or IFNγ+ CD3+ lymphocytes was analyzed in eight of them by flow cytometry. TNFα in sera was measured by ELISA in 11 patients. Results. A direct correlation was observed between resolution of AP lesions and an increase in IFNγ+ CD3+ peripheral blood mononuclear cells (P ≤ 0.001) and a decrease in TNFα serum levels (no statistical difference). No IL-4+ CD3+ cells were detected. Conclusions. Our findings confirm that AP is a disease that has an immunological component and that thalidomide clinical efficacy is exerted not only through inhibition of TNFα synthesis, but also through modulation of INFγ-producing CD3+ cells. These cells could be used as clinical markers for recovery.